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Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.

Pulmonary edema is cardiogenic and non-cardiogenic and is considered to be the immediate cause of death in every fourth deceased.

Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7–9 mm Hg. st., it is slightly higher than that in the interstitium. The fluid is retained in the capillaries due to its viscous properties, rather high oncotic pressure numbers. Alveolar capillary membranes are semi-permeable; the minimal flow of fluid from the pulmonary capillaries to the interstitium does not lead to pulmonary edema, since excess fluid immediately flows through the lymphatic vessels.

The occurrence of pulmonary edema requires the following factors:

• High hydrostatic pressure (more than 20-30 mm Hg. Art.) In the capillaries of the lungs. Such a hemodynamic situation is possible with acute left ventricular failure (myocardial infarction, post-infarction scars, tachyarrhythmias, etc.), mitral stenosis, large transfusions (transfusion of large quantities of fluids in reanimation, surgical practice, in pregnant women).

• Low, less than 15 mmHg. Art., oncotic pressure of plasma. This rarer cause of pulmonary edema is due to hypoproteinemia after blood loss, alimentary dystrophy, and hepatocellular insufficiency.

• High permeability of alveolar-capillary membranes in case of infectious-toxic, anaphylactic, enzymatic (pancreatic) shock, chemical and thermal trauma of the lungs, "neurogenic" pulmonary edema in stroke, severe traumatic brain injury.

• Negative (less than 20 mmHg) intraalveolar pressure with severe obstruction of the upper respiratory tract in patients with subglossal laryngitis, asphyxiation of tracheal foreign bodies;

when drowning; excessively active artificial respiration.

When pulmonary edema occurs, a self-sustaining tanatogenic vicious circle begins to “work”:

The variety of causes of pulmonary edema allows us to consider it a typical pathological process. Modern science has not answered the question of A. Sop-heim: is pulmonary edema the cause of death, or does pulmonary edema arise because the time has come for the patient to die (that is, the patient “dies through the mechanism of pulmonary edema”).

Cardiogenic pulmonary edema

Acute levorozh ud spectacle failure - cardiogenic interstitial and alveolar pulmonary edema - occurs with myocardial infarction, post-infarction cardiosclerosis, cardiomyopathy, acquired and congenital heart defects. The probability of acute left ventricular failure increases dramatically with max and systolic paroxysmal arrhythmias, hypertensive crises.

The left ventricle loses the ability to “pump” all the blood entering it during diastole, hence the increase in the final diastolic pressure in the left ventricle, hydrostatic pressure in the pulmonary veins, then in the capillaries and arteries. Due to the sharp increase in hydrostatic pressure in the pulmonary capillaries, the transudation of fluid in the interstitium increases, resorptive mechanisms become untenable. Interstitial pulmonary edema develops into alveolar. If the vicious circle of pulmonary edema (see above) cannot be broken, it is fatal.

Clinic, diagnosis. Interstitial pulmonary edema has a clinical equivalent in the form of a paroxysm of mixed dyspnea ("cardiac asthma"). The position of the patient is forced, half-sitting. Akrocyanosis. Tachypnea, tachycardia. In the lungs breathing weakened or hard, scattered dry rales. In patients with chronic heart failure under the scapulae, non-sounding finely bubbly moist rales can be heard.

Alveolar pulmonary edema is characterized by adherence to the described symptoms of moist rales starting from the roots of the lungs (interscapular spaces), then in all pulmonary fields. Breathing becomes bubbling, sometimes heard from a distance. With cough, frothy whitish-pink sputum is excreted. With auscultation of the heart - g-like rhythms. Tachycardia.

Radiographically with interstitial edema, the pulmonary pattern appears fuzzy, “blurred”. In the basal divisions decrease in transparency, expansion of interlobar partitions. In the basal-lateral departments and basal zones of the Curley line, peribronchial and perivascular shadows due to accumulation of transudate in the interstitial tissue.

The alveolar edema of the lungs from the standpoint of the X-ray method has several forms: central (with symmetric homogeneous dimming of high intensity in the central regions of the pulmonary fields); diffuse (with shadows of varying intensity); focal (with limited or confluent darkening of a rounded shape, capturing several segments or a lobe of the lung).

The course of pulmonary edema can be acute (up to 4 hours) with myocardial infarction, mitral stenosis, anaphylactic shock, cerebral stroke; subacute (4-12 h) - for myocardial infarction, acquired and congenital heart defects, pneumonia; prolonged (over 12 hours) - in patients with myocardial diseases, postinfarction cardiosclerosis, atrial fibrillation.

In the structure of the clinical diagnosis of pulmonary edema, cardiogenic and non-cardiogenic is always placed under the heading "complications of the underlying disease."

• CHD; Transmural peredneperegorodochny myocardial infarction (date, hour).

Complication. Cardiogenic alveolar pulmonary edema, acute course (date, hour).

• Rheumatism, inactive phase. Combined mitral defect with a predominance of stenosis of the left atrioventricular orifice. Atrial fibrillation, tachysystolic form.
Chronic heart failure 3 f. cl. (H 2 A).

Complication. Interstitial pulmonary edema, prolonged course (date, hour).

Urgent Care.

Universal life support methods:

- reassure the patient;

- if the arterial pressure is elevated or normal - give the patient a half-sitting position;

- inhalation of humidified oxygen through the nasal cannula. The mask is less acceptable, because in the state of suffocation, it is poorly tolerated;

- defoamers: inhalation of a 30% aqueous solution of ethyl alcohol or 2-3 ml of a 10% alcohol solution of anti-fomosilane. In severe cases, endotracheal administration of 2-4 ml of 96% ethanol solution;

- increase in resistance to breathing - exhalation through a tube dipped in a can of water;

- elimination of hypercatecholaminemia by introducing droperidol or Relanium, or narcotic analgesics into the vein.

Differentiated events:

• In case of toxic pulmonary edema (inhalation of phosgene, ozone, nitric oxide, cadmium oxide, monochloromethane, etc.; endotoxicosis in sepsis, peritonitis, meningococcal and non-clostridial anaerobic infections, pancreatitis, hantavirus-type pulmonary syndrome, in case of allergies, and in cases of non-inflammatory symptoms, in case of allergies, or in case of allergies; ) at the prehospital stage, prednisone is injected into a vein with a bolus of 90–120 mg, up to 1.2–2 g / day. For inhalation lesions, becotid or another inhaled glucocorticoid steroid, 4 breaths every 10 minutes until the inhaler is completely empty, calculated for 200-250 doses (V. Alekseev, V. Yakovlev, 1996).

To create an excessive gradient in order to direct the flow of fluid from the interstitium into the vascular bed, it is necessary to increase the plasma oncotic pressure. 10-20% albumin solution is injected into the vein to 200-400 ml / day. Immediate call to the emergency room of the ambulance. Intubation, artificial lung ventilation can save even patients with hantavirus pulmonary syndrome (OA Alekseev, VI Roshchupkin, 1997).

• In case of cardiogenic pulmonary edema, measures are determined by blood pressure (BP).

- If blood pressure is elevated, nitroglycerin is re-given sublingually, clonidine 0.25% 1-1.5 ml is injected intravenously in isotonic solution, lasix 40-80 mg, if necessary, re-morphine or Relanium. In severe cases, sodium nitroprusside 30 mg or nitroglycerin 5-10 mg intravenously. Sodium nitroprusside (naprprus, niprid) 30 mg in 400 ml of glucose begin to be injected at a speed of 6 drops / min with a gradual increase. Permanent control of blood pressure is obligatory, which should not fall to numbers below 90/60 mm Hg. Art! Side effects can be (except for hypotension) vomiting, abdominal pain, arrhythmias. The most convenient form of nitroglycerin for drip infusion into a vein is perlinganite ampoules containing 10 ml of a 0.1% solution of nitroglycerin in glucose (1 mg in 1 ml). A 0.01% solution is injected at an initial rate of 25 μg / min, which corresponds to 1 ml of a 0.01% solution in 4 minutes. Permanent control of blood pressure is required!

- At normal blood pressure numbers: sublingually repeated nitroglycerin, Lasix intramuscularly or intravenously at a dose of 40-80 mg, Relanium or morphine into a vein. In severe cases, intravenous nitroglycerin.

- The most severe clinical situation is pulmonary edema with low blood pressure. The position of the patient lying down. Dopamine intravenous drip: ampoules are used that contain 5 ml of a 0.5% solution (25 mg of dry matter) or 5 ml of a 4% solution (200 mg of dry matter). At 400 ml of 5% glucose, 200 mg of dopamine is added, the initial injection rate of 2-10 drops per minute.

An alternative option is the introduction of dobutamine. Dobutamine is available in 20 ml vials and 5 ml ampoules containing 250 mg of dry matter. The contents of the vial or ampoule is diluted in 400 ml of 5% glucose. The introduction of drip, the initial introduction rate of 5-10 cap. / Min. If long-term administration of dobutamine or dopamine is required, norepinephrine is added additionally (for 400 ml of liquid, 1 ml of a 0.1% solution of the preparation).

If you can increase blood pressure, are introduced lasix, nitroglycerin.

Specific clinical situations

• In case of myocardial infarction, good pain relief is necessary (fentanyl 0.005% 1-2 ml stream into a vein in combination with 2-4 ml of a 0.25% solution of droperidol). If the blood pressure numbers allow, an isoket is introduced into the vein (each ampoule contains 10 mg of dry matter in 10 ml of isotonic sodium chloride solution). The contents of 5 ampoules are added to 500 ml of infusible solution, the drug is injected drip into a vein, the initial speed is 3-7 drops / min, followed by a gradual increase. Permanent control of blood pressure is required!

• For paroxysmal tachyarrhythmias - universal anti-arrhythmic drugs (ethmozin, etatsizin, cordarone, procainamide, with ventricular tachycardia - 10-15 ml of 1% lidocaine solution, drip into a vein of panangin 20 ml, 4 U of simple insulin per 250 ml of 5% glucose). With the ineffectiveness of a single injection of an antiarrhythmic drug into a vein - electrical depolarization of the heart!

• In mitral stenosis, the method of choice is intravenous administration of morphine or its analogues, with normal or elevated blood pressure - 0.3-0.5-1 ml of pentamine or benzogeksoniya, depending on the numbers of blood pressure. With low blood pressure numbers, it is advisable to introduce 30-90 mg of prednisone into the vein.

The criteria for patient transportability after suffering pulmonary edema: the disappearance of frothy sputum, moist rales over all lung fields, the absence of a repeated suffocation attack in the horizontal position of the patient, the stabilization of the number of breaths 22-26 in 1 min. During transportation, inhalation of oxygen.
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Acute left ventricular failure - interstitial and alveolar pulmonary edema. Non-cardiogenic pulmonary edema.

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